RGD Reference Report - Complement 3 activates the KLF5 gene in rat vascular smooth muscle cells. - Rat Genome Database

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Complement 3 activates the KLF5 gene in rat vascular smooth muscle cells.

Authors: Yao, EH  Fukuda, N  Ueno, T  Tsunemi, A  Endo, M  Matsumoto, K 
Citation: Yao EH, etal., Biochem Biophys Res Commun. 2008 Mar 7;367(2):468-73. Epub 2008 Jan 4.
RGD ID: 5129534
Pubmed: PMID:18178156   (View Abstract at PubMed)
DOI: DOI:10.1016/j.bbrc.2007.12.160   (Journal Full-text)

We have shown that spontaneously hypertensive rat (SHR)-derived vascular smooth muscle cells (VSMCs) change to the synthetic phenotype and show increased expression of complement 3 (C3) and that C3 plays a role in the change to the synthetic phenotype. To determine the mechanisms underlying the effects of C3 on this phenotypic change, we examined the effects of C3a on transcription factors involved in VSMC phenotype and found that C3a increased the expression of Kruppel-like zinc-finger transcription factor 5 (KLF5) mRNA. C3a increased KLF5 promoter activity in a concentration-dependent manner. Deletion analysis of the promoter region of the KLF5 gene revealed that the region between nucleotides-991 and -699 contains the transcriptional regulatory element stimulated by C3a. C3a induced extracellular signal-regulated kinase (ERK) phosphorylation, and C3a-increased KLF5 promoter activity was completely inhibited by the MEK inhibitor U0126. These findings suggest that C3 increases KLF5 promoter activity and gene expression via ERK signaling.

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
positive regulation of ERK1 and ERK2 cascade  IDA 5129534 RGD 

Objects Annotated

Genes (Rattus norvegicus)
C3  (complement C3)


Additional Information